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铁缺乏与心力衰竭和慢性肾脏病的补充。

Iron deficiency and supplementation in heart failure and chronic kidney disease.

机构信息

Department of Medicine, Northwestern University, Chicago, IL, USA.

Department of Medicine, Northwestern University, Chicago, IL, USA; Feinberg Cardiovascular and Renal Research Institute, Northwestern University, Chicago, IL, USA.

出版信息

Mol Aspects Med. 2020 Oct;75:100873. doi: 10.1016/j.mam.2020.100873. Epub 2020 Aug 1.

DOI:10.1016/j.mam.2020.100873
PMID:32753256
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7554149/
Abstract

Iron is a key element for normal cellular function and plays a role in many cellular processes including mitochondrial respiration. The role of iron deficiency (ID) in heart failure (HF) has been a subject of debate amid increasing advocacy for intravenous (IV) supplementation. Both the definition and the approach to treatment of ID in HF have been adapted from the experience in patients with chronic kidney disease (CKD). In this review, we highlight the differences in regulatory mechanisms as well as pathophysiology of ID in CKD and HF population both at the systemic and cellular levels. We will review the major clinical trials in HF patients that have shown symptomatic benefit from IV iron supplementation but without effect on clinical outcomes. Intravenous iron loading bypasses the mechanisms that tightly regulate iron uptake and can potentially cause myocardial and endothelial damage by releasing reactive oxygen species. By contrast, newer oral iron preparations do not have similar toxicity concerns and might have a role in heart failure.

摘要

铁是细胞正常功能的关键元素,在许多细胞过程中发挥作用,包括线粒体呼吸。缺铁(ID)在心力衰竭(HF)中的作用一直是一个争议的话题,越来越多的人提倡静脉(IV)补充。HF 中 ID 的定义和治疗方法都借鉴了慢性肾脏病(CKD)患者的经验。在这篇综述中,我们强调了在系统性和细胞水平上,CKD 和 HF 人群中 ID 的调节机制和病理生理学的差异。我们将回顾 HF 患者的主要临床试验,这些试验表明 IV 铁补充有症状益处,但对临床结果没有影响。静脉内铁负荷绕过了严格调节铁摄取的机制,通过释放活性氧,可能导致心肌和内皮损伤。相比之下,新型口服铁制剂没有类似的毒性问题,可能在心力衰竭中发挥作用。

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